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Experimental study on the pathogenesis of cerebral aneurysms.

脑动脉瘤发病机制的实验研究。

基本信息

批准号：
61570168
负责人：
HAZAMA Fumitada
金额：
$ 1.54万
依托单位：
Shiga University of Medical Science
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1986
资助国家：
日本
起止时间：
1986 至 1988
项目状态：
已结题

项目摘要

The first purpose of the present study is to clarify the pathogenesis of cerebral aneurysms using our experimental model of the disease, and the second purpose is to induce aneurysms in the larger animals.1. Pathogenesis of experimentally induce cerbral aneurysms in ratsWe studied the early aneurysmal changes at the anterior cerebral artery/olfactory artery junction of rats treated with renal hypertension and ligation of the carotid artery.(1) The preaneurysmal changes occurred not at the apex istself, but on the distal side of the mafor branch abjacent to the apex. This fact casts doubt upon the medial defect theory for the development of cerebral aneurysms. (2) Various endothelial changes in the preaneurysmal portion seem to be the initiating change of the aneurysms formation. (3) Degeneration and disappearance of the internal elastic lamina observed at the preaneurysmal portion were suggested to be basic and pathogenetic changes of the development of aneurysms. (4) We found an increased activity of acid phosphatase at the preaneurysmal portion. Lysosomal enzymes seem to participate in the developmental mechanisms of cerbral aneurysms. (5) The factor XIII of blood coagulation proved to inhibit the development of aneurysms.2. Induction of cerebral aneurysms in monkeysWe succeeded in producing cerebral aneurysms in monkeys by treating them with renal hypertension, ligation of the common carotid artery and -aminopropionitrile feeding.

本研究的第一个目的是利用我们的疾病实验模型阐明脑动脉瘤的发病机制，第二个目的是在较大的动物中诱导动脉瘤。1．实验诱发大鼠脑动脉瘤的发病机制我们研究了肾性高血压和颈动脉结扎大鼠大脑前动脉/嗅动脉交界处的早期动脉瘤改变。(1)动脉瘤前改变不是发生在心尖本身，而是发生在心尖附近的mafor支的远端。这一事实对脑动脉瘤发展的内侧缺损理论提出了质疑。 (2)动脉瘤前部分的各种内皮变化似乎是动脉瘤形成的起始变化。 (3)动脉瘤前部观察到的内弹力层变性和消失被认为是动脉瘤发生发展的基本病理变化。 (4)我们发现动脉瘤前部分的酸性磷酸酶活性增加。溶酶体酶似乎参与脑动脉瘤的发育机制。 (5)凝血因子XIII具有抑制动脉瘤发展的作用。2．猴脑动脉瘤的诱导我们通过肾性高血压治疗、颈总动脉结扎和喂食β-氨基丙腈，成功地在猴体内产生了脑动脉瘤。